Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10513
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dc.contributor.authorBurchill, Luke Jen
dc.contributor.authorVelkoska, Elenaen
dc.contributor.authorDean, Rachael Gen
dc.contributor.authorLew, R Aen
dc.contributor.authorSmith, A Ien
dc.contributor.authorLevidiotis, Vickien
dc.contributor.authorBurrell, Louise Men
dc.date.accessioned2015-05-15T23:58:52Z
dc.date.available2015-05-15T23:58:52Z
dc.date.issued2008-01-25en
dc.identifier.citationExperimental Physiology 2008; 93(5): 622-30en
dc.identifier.govdoc18223026en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10513en
dc.description.abstractPatients with kidney failure are at high risk of a cardiac death and frequently develop left ventricular hypertrophy (LVH). The mechanisms involved in the cardiac structural changes that occur in kidney failure are yet to be fully delineated. Angiotensin-converting enzyme (ACE) 2 is a newly described enzyme that is expressed in the heart and plays an important role in cardiac function. This study assessed whether ACE2 plays a role in the cardiac remodelling that occurs in experimental acute kidney injury (AKI). Sprague-Dawley rats had sham (control) or subtotal nephrectomy surgery (STNx). Control rats received vehicle (n = 10), and STNx rats received the ACE inhibitor (ACEi) ramipril, 1 mg kg(-1) day(-1) (n = 15) or vehicle (n = 13) orally for 10 days after surgery. Rats with AKI had polyuria (P < 0.001), proteinuria (P < 0.001) and hypertension (P < 0.001). Cardiac structural changes were present and characterized by LVH (P < 0.001), fibrosis (P < 0.001) and increased cardiac brain natriuretic peptide (BNP) mRNA (P < 0.01). These changes occurred in association with a significant increase in cardiac ACE2 gene expression (P < 0.01) and ACE2 activity (P < 0.05). Ramipril decreased blood pressure (P < 0.001), LVH (P < 0.001), fibrosis (P < 0.01) and BNP mRNA (P < 0.01). These changes occurred in association with inhibition of cardiac ACE (P < 0.05) and a reduction in cardiac ACE2 activity (P < 0.01). These data suggest that AKI, even at 10 days, promotes cardiac injury that is characterized by hypertrophy, fibrosis and increased cardiac ACE2. Angiotensin-converting enzyme 2, by promoting the production of the antifibrotic peptide angiotensin(1-7), may have a cardioprotective role in AKI, particularly since amelioration of adverse cardiac effects with ACE inhibition was associated with normalization of cardiac ACE2 activity.en
dc.language.isoenen
dc.subject.otherAcute Kidney Injury.enzymology.genetics.pathologyen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherAutoradiographyen
dc.subject.otherBlood Pressure.physiologyen
dc.subject.otherBody Weight.drug effectsen
dc.subject.otherCollagen.metabolismen
dc.subject.otherDrinking.physiologyen
dc.subject.otherFluorescent Dyesen
dc.subject.otherGene Expression Regulation, Enzymologic.physiologyen
dc.subject.otherHeart Function Testsen
dc.subject.otherHeart Rate.physiologyen
dc.subject.otherKidney Function Testsen
dc.subject.otherMyocardium.enzymology.pathologyen
dc.subject.otherNephrectomyen
dc.subject.otherPeptidyl-Dipeptidase A.biosynthesisen
dc.subject.otherProteinuria.etiologyen
dc.subject.otherRNA, Messenger.biosynthesis.geneticsen
dc.subject.otherRatsen
dc.subject.otherReverse Transcriptase Polymerase Chain Reactionen
dc.subject.otherUrodynamics.physiologyen
dc.subject.otherVentricular Remodeling.physiologyen
dc.titleAcute kidney injury in the rat causes cardiac remodelling and increases angiotensin-converting enzyme 2 expression.en
dc.typeJournal Articleen
dc.identifier.journaltitleExperimental physiologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria 3081, Australiaen
dc.identifier.doi10.1113/expphysiol.2007.040386en
dc.description.pages622-30en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/18223026en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
crisitem.author.deptCardiology-
crisitem.author.deptGeneral Medicine-
crisitem.author.deptMedicine (University of Melbourne)-
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